Furanocoumarin Phytoalexins, Trichothecene Toxins, and Infection ofPastinaca sativabyFusarium sporotrichioides

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Abstract
Many plant pathogenic fusaria produce trichotecenes, which are potent phytotoxins and inhibitors of protein synthesis in eukaryotes. In this study we show that a wild-type, trichotecene-producing strain of F. sporotrichioides, NRRL 3299, is pathogenic on Pastinacca sativa (parsnip) roots and produces T-2 toxin in planta. Parsnip roots infected with this strain also accumulate high levels of fungitoxic furanocoumarins, mainly xanthotoxin and angelicin. Analysis of serial sections of infected roots showed that furanocoumarin concentrations decrease sharply at the infection boundary to levels apparently insufficient to completely block fungal growth or trichothecene production. The involvement of trichothecenes in pathogenesis was investigated by using three previously isolated, complementary mutants of NRRL 3299, blocked at different steps in T-2 toxin biosynthesis, T-2 toxin production is restored when these mutants are grown together pairwise and each mutant accumulates different end products. In this study the ability of these mutants to infect parsnips correlates with their ability to produce certain trichothecenes. Thus, the mutant that accumulates 4,15-diacetoxyscirpenol, a trichothecene nearly as toxic as T-2 toxin, is as pathogenic as the wild-type parent. In contrast, neither the mutant that accumulates the less toxic calonectrin analogues nor the mutant that accumulates the nontoxic trichothecene precursor, trichodiene, is pathogenic. Furthermore, coinoculation of these latter two mutants on parsnip roots results in infection.